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Open AccessJournal ArticleDOI

The endoplasmic reticulum and the unfolded protein response.

TLDR
The endoplasmic reticulum is the site where proteins enter the secretory pathway, and those processes that prevent accumulation of unfolded proteins in the ER lumen are highly regulated by an intracellular signaling pathway known as the unfolded protein response (UPR).
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This article is published in Seminars in Cell & Developmental Biology.The article was published on 2007-12-01 and is currently open access. It has received 960 citations till now. The article focuses on the topics: Unfolded protein response & Endoplasmic reticulum.

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Citations
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Cell death and endoplasmic reticulum stress: disease relevance and therapeutic opportunities

TL;DR: The accumulation of unfolded proteins in the endoplasmic reticulum represents a cellular stress induced by multiple stimuli and pathological conditions, which triggers an evolutionarily conserved series of signal-transduction events, which constitutes the unfolded protein response.
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Defining the Human Deubiquitinating Enzyme Interaction Landscape

TL;DR: A global proteomic analysis of Dubs and their associated protein complexes provided the first glimpse into the Dub interaction landscape, places previously unstudied Dubs within putative biological pathways, and identifies previously unknown interactions and protein complexes involved in this increasingly important arm of the ubiquitin-proteasome pathway.
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Biological and Chemical Approaches to Diseases of Proteostasis Deficiency

TL;DR: It is proposed that small molecules can enhance proteostasis by binding to and stabilizing specific proteins (pharmacologic chaperones) or by increasing the protestasis network capacity (proteostasis regulators) and that such therapeutic strategies, including combination therapies, represent a new approach for treating a range of diverse human maladies.
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Calcium and ROS: A mutual interplay.

TL;DR: Increasing evidence suggests a mutual interplay between calcium and ROS signaling systems which seems to have important implications for fine tuning cellular signaling networks.
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PERK is required at the ER-mitochondrial contact sites to convey apoptosis after ROS-based ER stress

TL;DR: It is revealed that PERK (RNA-dependent protein kinase (PKR)-like ER kinase), a key ER stress sensor of the unfolded protein response, is uniquely enriched at the mitochondria-associated ER membranes (MAMs), suggesting that loss of PERK may cause defects in cell death sensitivity in pathological conditions linked to ROS-mediated ER stress.
References
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Journal ArticleDOI

Atherosclerosis — An Inflammatory Disease

TL;DR: Atherosclerosis is an inflammatory disease as discussed by the authors, and it is a major cause of death in the United States, Europe, and much of Asia, despite changes in lifestyle and use of new pharmacologic approaches to lower plasma cholesterol concentrations.
Journal Article

Atherosclerosis is an Inflammatory Disease

TL;DR: Despite changes in lifestyle and the use of new pharmacologic approaches to lower plasma cholesterol concentrations, cardiovascular disease continues to be the principal cause of death in the United States, Europe, and much of Asia.
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Calcium signalling: dynamics, homeostasis and remodelling

TL;DR: The Ca2+-signalling toolkit is used to assemble signalling systems with very different spatial and temporal dynamics and has a direct role in controlling the expression patterns of its signalling systems that are constantly being remodelled in both health and disease.
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Insulin signalling and the regulation of glucose and lipid metabolism

TL;DR: The epidemic of type 2 diabetes and impaired glucose tolerance is one of the main causes of morbidity and mortality worldwide, and tissues such as muscle, fat and liver become less responsive or resistant to insulin.
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Endothelial Dysfunction in Cardiovascular Diseases: The Role of Oxidant Stress

TL;DR: Accumulating evidence suggests that oxidant stress alters many functions of the endothelium, including modulation of vasomotor tone, and as the role of these various enzyme sources of ROS become clear, it will perhaps be possible to use more specific therapies to prevent their production and ultimately correct endothelial dysfunction.
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